Systemic phlorizin prevents gold thioglucose necrosis in the ventromedial hypothalamus.
Intraventricular and intrahypothalamic infusions of phlorizin (PHL) are known to cause hyperphagia and to prevent gold thioglucose (GTG) lesion formation in the ventromedial hypothalamus (VMH), respectively. In this study, PHL, administered IP in a large dose (900 mg/kg), completely inhibited GTG necrosis in the VMH. PHL did not cause excessive urinary excretion of GTG. This evidence suggested that systemic PHL must be injected in a high concentration to alter the hypothalamic response to GTG. In vitro measurements of VMH glucose oxidation substantiated this idea. Only at a high concentration of PHL was glucose oxidation significantly depressed in the VMH (p less than 0.001). Small amounts of PHL elevated VMH glucose oxidation (p less than 0.001). Since PHL is an inhibitor of glucose transport, these data support the concept of a hypothalamic glucostatic modulation for the control of food intake.
D000818:Animals; D006051:Aurothioglucose / Q000633:toxicity*; D005260:Female; D006046:Gold / Q000633:toxicity*; D007031:Hypothalamus / Q000187:drug effects / Q000473:pathology*; D008473:Median Eminence / Q000502:physiology; D051379:Mice; D009336:Necrosis; D010695:Phlorhizin / Q000494:pharmacology*
D006051:Aurothioglucose; D006046:Gold; D010695:Phlorhizin